Extrasystoles I49.4

Synonyms

Premature heartbeat; premature systole; premature contractions; cardiac stutter; contraction outside normal heart rhythm; AV nodal ES; junctional ES; sinus ES; atrial ES; aberrant SVES; premature atrial contractions; PAC; premature supraventricular beat; premature atrial beat; premature supraventricular complexes; atrial premature complexes; premature ventricular beats; premature ventricular contractions; PVC;

First author

Cardiologist Bernhard Lown, born in 1921, achieved the first successful cardioversion for atrial fibrillation in 1963 (Weber 2018).

The classification of ventricular extrasystoles was developed by Bernhard Lown in 1971 and named after him as the "Lown classification" (Weber 2018).

Scherf and Scott defined extrasystoles in 1953 as "contraction of the whole or part of the heart, starting from an impulse that is abnormal, either in its origin (ectopic) or in the time of occurrence (premature), or both. The extrasystole interferes with the dominant rhythm and has a constant following distance from the preceding beat when it occurs repeatedly" (Roskamm 2013).

Extrasystoles (ES) belong to the heterotopic stimulation disorders (Herold 2022).

One differentiates - depending on the origin of the excitation - between:

- Supraventricular extrasystoles (SVES).

SVES originate in the sinus node, atrium or AV node (Striebel 2015).

- Ventricular extrasystoles (VES).

VES arise below the bifurcation of the His- bundle (Herold 2022), predominantly in the peripheral or proximal His- Purkinje system (Wolff 2012).

ES can be monomorphic / polymorphic. This refers to an identical / different configuration in the ECG. They can also be monotopic / polytopic, involving an identical / different center of excitation (Roskamm 2013).

ES are very common, even in healthy individuals (Herold 2022). The most common form of arrhythmia is ventricular extrasystoles(Gertsch 2008).

Pregnant women have a high incidence of extrasystoles, both atrial and ventricular (Rath 2005).

The causes for the occurrence of extrasystoles can be very different:

- Idiopathic (Ip 2017)

- Physiological reasons:

These are also found in healthy individuals. Here, extrasystoles occur due to increased sympathetic tone (Kasper 2015), emotional arousal, autonomic lability, overtiredness, ingestion of stimulants such as alcohol, nicotine, caffeine, increased vagotone, etc (Herold 2022).

- Organic diseases of the heart:

These include cardiomyopathies, myocarditis, coronary artery disease (Herold 2022), cardiac tumors, congenital heart defects (Paul 2018).

- Extracardiac Causes:

Extracardiac causes include hyperthyroidism, hypokalemia, use of certain medications such as. Antiarrhythmics, sympathomimetics, digitalis, tricyclic antidepressants (Herold 2022), catecholamines, quinidine, atropine, antiarrhythmics (Wolff 2012), fever, infections (van Aken 2007), acidosis, hypoxia, electrolyte disturbances, especially hypokalemia, hypercalcemia, hypomagnesemia (Haas 2021).

Extrasystoles may occur due to automatism or reentry (Kasper 2015).

The electrophysiological properties such as the action potential, the distribution of Ca2+ and Na+ channels change strongly along the His bundle. From this point of view, the electrophysiological boundary between VES and SVES cannot be drawn precisely.

From a clinical point of view, the His- bundle is referred to as supraventricular because additional excitations from this area lead to normal QRS- complexes (Roskamm 2013).

- SVES:

In this case, the premature contraction covers the entire heart and usually shows atrial and ventricular complexes in the ECG in mutual relation and normal ventricular complexes, since the extra stimulus originates above the His- bundle and can therefore propagate from there along normal conduction pathways into the chambers of the myocardium (Roskamm 2013).

- VES:

VES, on the other hand, involves premature contraction of the chambers alone. Depolarization occurs first in the chamber in which the VES originates and only then in the other chamber. The ECG shows a dissociated and deformed ventricular complex (Roskamm 2013) because excitation propagation away from the ventricular focus through the ventricular myocardium is slower than activation of the ventricles by the Purkinje system. This results in a QRS complex that is typically widened to > 0.12 s (Kasper 2015).

Extrasystoles can occur at any age, even in children (Paul 2018).

The site of origin of the ES may be:

- cranial of the His bundle

- in the His bundle

- distal of the His bundle (Roskamm 2013)

SVES can originate from the:

- sinus node

- atrium

- AV node (Striebel 2015)

They always originate above the His bundle (van Aken 2007)

VES can originate:

- from the focus of myocardial or Purkinje cells, which are capable of automatism

- from a triggered automaticity

- from a re-entry through areas with scars

- through a diseased Purkinje system (Kasper 2015).

VES always arise distal to the His bundle (van Aken 2007).

Extrasystoles are noticed as palpitation by about 30 % of the affected persons. They report cardiac stuttering or interruptions as symptoms. Only a part of them feels ill by the extrasystoles (Herold 2022).

Symptoms may include:

- Feeling of weakness

- Dizziness (Braun 2022)

- Cardiac syncope / presyncope (Kasper 2015).

- Palpitations (Herold 2022)

- Dyspnea (Meismann 2021)

Since extrasystoles cause an unconscious reaction of the autonomic nervous system, palpitations can trigger an anxiety reaction up to a panic attack in affected persons. These patients may complain of dyspnea, chest tightness, etc. (Meismann 2021).

The presence of ES is usually first detected on a resting ECG. Recording with a 12-lead ECG is then recommended (Kasper 2015).

In particular, any cardiomyopathies or sudden deaths should be asked about in the family history (Kasper 2015).

This should be followed by a long-term ECG for further quantification. Additional diagnostics consist of ergometry, echocardiography (Herold 2022) and, if necessary, cardiac MRI (Braun 2019).

- 12- channel ECG

SVES are characterized in the ECG by:

- change of the PQ- time (Herold 2022)

- premature collapse of the P-wave

- slight deformation of the P-wave

- the cardiac action following the ES shows no compensatory pause (Block 2006).

- negative P in II, III, aVF:

Arises from SVES originating in the inferior segment of the atrium and leading to caudo-cranial excitation of the atrium. Occurs in atrial ES and nodal ES (Haas 2011).

- Negative P in I and aVL:

May occur in nodal ES (Haas 2011). This is an SVES with left atrial origin (Schuster 2005).

- P- wave before, in, or after the QRS complex:

These changes result from retrograde excitation of the atria. They may occur in nodal ES (Haas 2011).

- QRS- complex:

The QRS- complex of an SVES is normal in shape and width in most cases (Block 2006), and the QRS- duration is < 120 ms (Kasper 2015). The only exception is early-onset SVES - also known as aberrant SVES (Herold 2022). In this case, the excitation runs over the AV node and encounters a still refractory Tawara limb. Due to this blockage, an abnormal propagation of the excitation into the ventricles takes place, resulting in a widened QRS morphology (Kalkreuth 2013).

- PR- interval:

This may be shortened, normal, or prolonged (Heaton 2022).

In VES, the ECG may typically show:

- Absence of P-wave (in the predominant cases).

- widening of the QRS complexes deformed like a branch block (Haas 2011)

- prematurely incident QRS complexes (Braun 2022)

- discordant T-wave

- VES is followed by a compensatory pause (Braun 2022)

- fusion beat (Haas 2011):

Here, simultaneous excitation of the ventricles by a supraventricular and a ventricular center leads to the occurrence of a fusion beat. Recognizable in the ECG by simultaneous SVES and VES changes (Gertsch 2008).

- Long-term ECG

Here, the frequency of ES can be clarified, as well as any occurrence of volleys, tachycardia, intermittent atrial fibrillation or atrial flutter (Haas 2011 / Greten 2010).

For more details, see VES and SVES.

- Ergometry

In case of V. a. exercise-induced ES or coronary artery disease, ergometry should be performed (Kasper 2015). For more information, see also VES and SVES.

- Echocardiography

This should be performed to rule out structural heart disease (Heaton 2022).

For more details, see VES and SVES.

- Cardiac magnetic resonance imaging

Cardiac MRI is required only in certain cases. It is used to assess cardiac structure, cardiac function, and characterize myocardial tissue (Muser 2021).

For more details see VES

- Checking the electrolytes (Heaton 2022) especially K, Mg, Ca

- CK / CK- MB

- Troponin I

- TSH

- Checking certain drug levels such as digitalis

- Drug screening (Haas 2011)

s. VES and SVES

- (Reversible) cardiomyopathy

- Decrease in ventricular function

- Ventricular dilatation (Latchamsetty 2019)

- Heart failure (Marcus 2020)

- Tachycardia (Haas 2011)

- Ischemic apoplexy (Heaton 2022)

- Sudden cardiac death (Marcus 2020)

For more details see VES and SVES

Therapy is not required for all forms of ES.

Depending on the type of ES, symptomatic therapy may consist of:

- Checking potassium and magnesium balance with possible substitution up to high-normal serum levels (Herold 2022).

- Avoidance of certain triggers such as alcohol, nicotine, coffee, overtiredness, emotional arousal, cocaine (Herold 2022 / Haas 2011).

- If necessary, correction of drug levels (especially with digitalis [Wolff 2012]).

Medicinally, antiarrhythmic drugs may be considered under certain conditions.

Indications may be:

- Increased risk of sudden cardiac death due to e.g. ventricular fibrillation.

- complex ES in patients with restriction of left ventricular pump function or severe underlying myocardial disease (Herold 2022)

- symptomatic (idiopathic) ES (Muser 2021 / Heaton 2022)

- frequently occurring ES

- echocardiographic evidence of left ventricular dysfunction

- Occurrence of warning arrhythmias, ie:

- Occurrence of volley-like VES with limitations in exercise capacity.

- occurrence of syncope (Braun 2022)

For more details see VES and SVES.

Dosage and choice of antiarrhythmic drug:

- Beta blocker

Antiarrhythmics of 1st choice are beta blockers without intrinsic sympathomimetic activity for patients with impaired pumping capacity and Z. n. myocardial infarction (Herold 2022).

- Calcium channel blockers

If beta-blockers do not produce the desired outcome, therapy with non-dihydropyridine calcium channel blockers is indicated. The lowest effective dose should be used, except in patients with recent myocardial infarction or existing heart failure. Here, the maximum tolerated dose should be titrated (Muser 2021).

- Sodium channel blockers.

If therapeutic success cannot be achieved with both beta blockers and calcium channel blockers, therapy with sodium channel blockers such as flecainide or propafenone is recommended. However, sodium channel blockers are contraindicated in the presence of existing coronary artery disease, heart failure, or severe left ventricular hypertrophy (Muser 2021).

- Amiodarone

In patients with VES-induced cardiomyopathy, amiodarone has been shown to improve symptoms and left ventricular function (Muser 2021)

In patients with structural heart disease such as heart failure, CHD, class I antiarrhythmic drugs are contraindicated because they may worsen prognosis in them. Similarly, amiodarone and sotalol show no prognostic advantage, even leading to worsening of prognosis in patients with NYHA III . In all these cases, an implantable cardioverter- defibrillator (ICD) is recommended (Herold 2022).

In patients with cardiomyopathy, heart failure, atrial fibrillation, etc. associated with ES, further interventional therapy is indicated. These include atrial pacing, catheter ablation (Heaton 2022), radiofrequency catheter ablation (Muser 2021), thoracoscopic ablation (Heaton 2022), implantation of a defibrillator (Braun 2022).

For more details see VES and SVES.

The prognosis depends on the type of ES.

SVES:

In earlier years, supraventricular extrasystoles-unless structural heart disease was present-were thought to be harmless, requiring no therapy (Rath 2005). Meanwhile, increasing evidence implicates the role of symptomatic (clustered) SVES with atrial fibrillation and apoplexy. However, further research is needed in this regard (Marcus 2015).

Clustered SVES may be associated with the development of atrial fibrillationor atrial flutter and thus with an increased risk of cardiac mortality or increase in all-cause mortality (Heaton 2022). For more details see SVES

VES:

Idiopathic VES can induce (reversible) cardiomyopathy, as well as trigger ventricular fibrillation in susceptible patients via polymorphic ventricular tachycardia, thus causing sudden cardiac death, contrary to earlier assumptions (Ip 2017).

The long-term prognosis of idiopathic VES without structural heart disease is good (Muser 2021). Patients with preexisting heart failure show increased mortality when VES occurs (Kasper 2015). For more details see VES

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